Updated on 2024/07/13

写真a

 
ITO Yasuyuki
 
Organization
Academic Assembly Institute of Medicine and Dentistry IGAKU KEIRETU Assistant Professor
Faculty of Medicine School of Medicine Assistant Professor
Graduate School of Medical and Dental Sciences Molecular and Cellular Medicine Signal Transduction Research Assistant Professor
Title
Assistant Professor
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Degree

  • 博士(医学) ( 2013.4   大阪大学 )

Research Interests

  • 神経

  • リン酸化プロテオミクス

  • 結晶構造解析

  • 発生

  • 細胞生物

Research Areas

  • Life Science / Neuroscience-general

  • Life Science / Structural biochemistry

  • Life Science / Cell biology

Research History

  • Niigata University   Faculty of Medicine School of Medicine   Assistant Professor

    2013.4

  • Niigata University   Graduate School of Medical and Dental Sciences Molecular and Cellular Medicine Signal Transduction Research   Assistant Professor

    2013.4

 

Papers

  • Identification of the growth cone as a probe and driver of neuronal migration in the injured brain. International journal

    Chikako Nakajima, Masato Sawada, Erika Umeda, Yuma Takagi, Norihiko Nakashima, Kazuya Kuboyama, Naoko Kaneko, Satoaki Yamamoto, Haruno Nakamura, Naoki Shimada, Koichiro Nakamura, Kumiko Matsuno, Shoji Uesugi, Nynke A Vepřek, Florian Küllmer, Veselin Nasufović, Hironobu Uchiyama, Masaru Nakada, Yuji Otsuka, Yasuyuki Ito, Vicente Herranz-Pérez, José Manuel García-Verdugo, Nobuhiko Ohno, Hans-Dieter Arndt, Dirk Trauner, Yasuhiko Tabata, Michihiro Igarashi, Kazunobu Sawamoto

    Nature communications   15 ( 1 )   1877 - 1877   2024.3

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    Axonal growth cones mediate axonal guidance and growth regulation. We show that migrating neurons in mice possess a growth cone at the tip of their leading process, similar to that of axons, in terms of the cytoskeletal dynamics and functional responsivity through protein tyrosine phosphatase receptor type sigma (PTPσ). Migrating-neuron growth cones respond to chondroitin sulfate (CS) through PTPσ and collapse, which leads to inhibition of neuronal migration. In the presence of CS, the growth cones can revert to their extended morphology when their leading filopodia interact with heparan sulfate (HS), thus re-enabling neuronal migration. Implantation of an HS-containing biomaterial in the CS-rich injured cortex promotes the extension of the growth cone and improve the migration and regeneration of neurons, thereby enabling functional recovery. Thus, the growth cone of migrating neurons is responsive to extracellular environments and acts as a primary regulator of neuronal migration.

    DOI: 10.1038/s41467-024-45825-8

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  • Very-long-chain fatty acids are crucial to neuronal polarity by providing sphingolipids to lipid rafts. International journal

    Atsuko Honda, Motohiro Nozumi, Yasuyuki Ito, Rie Natsume, Asami Kawasaki, Fubito Nakatsu, Manabu Abe, Haruki Uchino, Natsuki Matsushita, Kazutaka Ikeda, Makoto Arita, Kenji Sakimura, Michihiro Igarashi

    Cell reports   113195 - 113195   2023.10

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    Fatty acids have long been considered essential to brain development; however, the involvement of their synthesis in nervous system formation is unclear. We generate mice with knockout of GPSN2, an enzyme for synthesis of very-long-chain fatty acids (VLCFAs) and investigate the effects. Both GPSN2-/- and GPSN2+/- mice show abnormal neuronal networks as a result of impaired neuronal polarity determination. Lipidomics of GPSN2-/- embryos reveal that ceramide synthesis is specifically inhibited depending on FA length; namely, VLCFA-containing ceramide is reduced. We demonstrate that lipid rafts are highly enriched in growth cones and that GPSN2+/- neurons lose gangliosides in their membranes. Application of C24:0 ceramide, but not C16:0 ceramide or C24:0 phosphatidylcholine, to GPSN2+/- neurons rescues both neuronal polarity determination and lipid-raft density in the growth cone. Taken together, our results indicate that VLCFA synthesis contributes to physiological neuronal development in brain network formation, in particular neuronal polarity determination through the formation of lipid rafts.

    DOI: 10.1016/j.celrep.2023.113195

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  • Correction to: JNK1‑Dependent Phosphorylation of GAP‑43 Serine 142 is a Novel Molecular Marker for Axonal Growth. International journal

    Masayasu Okada, Yosuke Kawagoe, Toshiyuki Takasugi, Motohiro Nozumi, Yasuyuki Ito, Hayato Fukusumi, Yonehiro Kanemura, Yukihiko Fujii, Michihiro Igarashi

    Neurochemical research   47 ( 9 )   2683 - 2683   2022.9

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  • JNK1-Dependent Phosphorylation of GAP-43 Serine 142 is a Novel Molecular Marker for Axonal Growth. International journal

    Masayasu Okada, Yosuke Kawagoe, Toshiyuki Takasugi, Motohiro Nozumi, Yasuyuki Ito, Hayato Fukusumi, Yonehiro Kanemura, Yukihiko Fujii, Michihiro Igarashi

    Neurochemical research   47 ( 9 )   2668 - 2682   2022.3

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    Mammalian axon growth has mechanistic similarities with axon regeneration. The growth cone is an important structure that is involved in both processes, and GAP-43 (growth associated protein-43 kDa) is believed to be the classical molecular marker. Previously, we used growth cone phosphoproteomics to demonstrate that S96 and T172 of GAP-43 in rodents are highly phosphorylated sites that are phosphorylated by c-jun N-terminal protein kinase (JNK). We also revealed that phosphorylated (p)S96 and pT172 antibodies recognize growing axons in the developing brain and regenerating axons in adult peripheral nerves. In rodents, S142 is another putative JNK-dependent phosphorylation site that is modified at a lower frequency than S96 and T172. Here, we characterized this site using a pS142-specific antibody. We confirmed that pS142 was detected by co-expressing mouse GAP-43 and JNK1. pS142 antibody labeled growth cones and growing axons in developing mouse neurons. pS142 was sustained until at least nine weeks after birth in mouse brains. The pS142 antibody could detect regenerating axons following sciatic nerve injury in adult mice. Comparison of amino acid sequences indicated that rodent S142 corresponds to human T151, which is predicted to be a substrate of the MAPK family, which includes JNK. Thus, we confirmed that the pS142 antibody recognized human phospho-GAP-43 using activated JNK1, and also that its immunostaining pattern in neurons differentiated from human induced pluripotent cells was similar to those observed in mice. These results indicate that the S142 residue is phosphorylated by JNK1 and that the pS142 antibody is a new candidate molecular marker for axonal growth in both rodents and human.

    DOI: 10.1007/s11064-022-03580-6

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  • Phosphorylation sites of microtubule-associated protein 1B (MAP 1B) are involved in axon growth and regeneration. Reviewed International journal

    Ishikawa Y, Okada M, Honda A, Ito Y, Tamada A, Endo N, Igarashi M

    Molecular brain   12 ( 1 )   93 - 93   2019.11

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    The growth cone is a specialized structure that forms at the tip of extending axons in developing and regenerating neurons. This structure is essential for accurate synaptogenesis at developmental stages, and is also involved in plasticity-dependent synaptogenesis and axon regeneration in the mature brain. Thus, understanding the molecular mechanisms utilized by growth cones is indispensable to understanding neuronal network formation and rearrangement. Phosphorylation is the most important and commonly utilized protein modification in signal transduction. We previously identified microtubule-associated protein 1B (MAP 1B) as the most frequently phosphorylated protein among ~ 1200 phosphorylated proteins. MAP 1B has more than 10 phosphorylation sites that were present more than 50 times among these 1200 proteins. Here, we produced phospho-specific antibodies against phosphorylated serines at positions 25 and 1201 of MAP 1B that specifically recognize growing axons both in cultured neurons and in vivo in various regions of the embryonic brain. Following sciatic nerve injury, immunoreactivity with each antibody increased compared to the sham operated group. Experiments with transected and sutured nerves revealed that regenerating axons were specifically recognized by these antibodies. These results suggest that these MAP 1B phosphorylation sites are specifically involved in axon growth and that phospho-specific antibodies against MAP 1B are useful markers of growing/regenerating axons.

    DOI: 10.1186/s13041-019-0510-z

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  • Growth Cone Phosphoproteomics Reveals that GAP-43 Phosphorylated by JNK Is a Marker of Axon Growth and Regeneration. Reviewed International journal

    Asami Kawasaki, Masayasu Okada, Atsushi Tamada, Shujiro Okuda, Motohiro Nozumi, Yasuyuki Ito, Daiki Kobayashi, Tokiwa Yamasaki, Ryo Yokoyama, Takeshi Shibata, Hiroshi Nishina, Yutaka Yoshida, Yukihiko Fujii, Kosei Takeuchi, Michihiro Igarashi

    iScience   4   190 - 203   2018.6

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    Neuronal growth cones are essential for nerve growth and regeneration, as well as for the formation and rearrangement of the neural network. To elucidate phosphorylation-dependent signaling pathways and establish useful molecular markers for axon growth and regeneration, we performed a phosphoproteomics study of mammalian growth cones, which identified >30,000 phosphopeptides of ∼1,200 proteins. The phosphorylation sites were highly proline directed and primarily MAPK dependent, owing to the activation of JNK, suggesting that proteins that undergo proline-directed phosphorylation mediate nerve growth in the mammalian brain. Bioinformatics analysis revealed that phosphoproteins were enriched in microtubules and the cortical cytoskeleton. The most frequently phosphorylated site was S96 of GAP-43 (growth-associated protein 43-kDa), a vertebrate-specific protein involved in axon growth. This previously uncharacterized phosphorylation site was JNK dependent. S96 phosphorylation was specifically detected in growing and regenerating axons as the most frequent target of JNK signaling; thus it represents a promising new molecular marker for mammalian axonal growth and regeneration.

    DOI: 10.1016/j.isci.2018.05.019

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  • Glycoprotein M6a as a signaling transducer in neuronal lipid rafts. Reviewed

    Ito Y, Honda A, Igarashi M

    Neuroscience research   128   19 - 24   2018.3

  • Extracellular Signals Induce Glycoprotein M6a Clustering of Lipid Rafts and Associated Signaling Molecules Reviewed

    Atsuko Honda, Yasuyuki Ito, Kazuko Takahashi-Niki, Natsuki Matsushita, Motohiro Nozumi, Hidenori Tabata, Kosei Takeuchi, Michihiro Igarashi

    JOURNAL OF NEUROSCIENCE   37 ( 15 )   4046 - 4064   2017.4

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:SOC NEUROSCIENCE  

    Lipid raft domains, where sphingolipids and cholesterol are enriched, concentrate signaling molecules. Toexaminehowsignaling protein complexes are clustered in rafts, we focused on the functions of glycoprotein M6a (GPM6a), which is expressed at a high concentration in developing mouse neurons. Using imaging of lipid rafts, we found that GPM6a congregated in rafts in a GPM6a palmitoylation-dependent manner, thereby contributing to lipid raft clustering. In addition, we found that signaling proteins downstream of GPM6a, such as Rufy3, Rap2, and Tiam2/STEF, accumulated in lipid rafts in a GPM6a-dependent manner and were essential for laminin-dependent polarity during neurite formation in neuronal development. In utero RNAi targeting of GPM6a resulted in abnormally polarized neurons with multiple neurites. These results demonstrate that GPM6a induces the clustering of lipid rafts, which supports the raft aggregation of its associated downstream molecules for acceleration of neuronal polarity determination. Therefore, GPM6a acts as a signal transducer that responds to extracellular signals.

    DOI: 10.1523/JNEUROSCI.3319-16.2017

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  • The four-transmembrane protein IP39 of Euglena forms strands by a trimeric unit repeat Reviewed

    Hiroshi Suzuki, Yasuyuki Ito, Yuji Yamazaki, Katsuhiko Mineta, Masami Uji, Kazuhiro Abe, Kazutoshi Tani, Yoshinori Fujiyoshi, Sachiko Tsukita

    NATURE COMMUNICATIONS   4   1766   2013.4

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    Euglenoid flagellates have striped surface structures comprising pellicles, which allow the cell shape to vary from rigid to flexible during the characteristic movement of the flagellates. In Euglena gracilis, the pellicular strip membranes are covered with paracrystalline arrays of a major integral membrane protein, IP39, a putative four-membrane-spanning protein with the conserved sequence motif of the PMP-22/EMP/MP20/Claudin superfamily. Here we report the three-dimensional structure of Euglena IP39 determined by electron crystallography. Two-dimensional crystals of IP39 appear to form a striated pattern of antiparallel double-rows in which trimeric IP39 units are longitudinally polymerised, resulting in continuously extending zigzag-shaped lines. Structural analysis revealed an asymmetric molecular arrangement in the trimer, and suggested that at least four different interactions between neighbouring protomers are involved. A combination of such multiple interactions would be important for linear strand formation of membrane proteins in a lipid bilayer.

    DOI: 10.1038/ncomms2731

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  • Phosphodiesterase isozymes involved in regulating acid secretion in the isolated mouse stomach. Reviewed

    S. Okuda, M. Honda, Y. Ito, E. Aihara, S. Kato, S. Mitsufuji, T. Yoshikawa, K. Takeuchi

    Journal of physiology and pharmacology : an official journal of the Polish Physiological Society   60 Suppl 7   183 - 190   2009.12

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    The effect of subtype-selective phosphodiesterase (PDE) inhibitors on acid secretion was examined in mouse stomachs to investigate which PDE isozymes are involved in the local regulation of this secretion. Male DDY mice were used after 18 h fasting. An isolated stomach was incubated in an organ bath containing buffered solution gassed with 95% O(2)/5% CO(2), while the lumen was perfused with unbuffered solution gassed with 100% O(2). Acid secretion was measured at pH 5.4 using a pH-stat method. Histamine or pituitary adenylate cyclase activating polypeptide (PACAP) was added to the serosal solution. PDE inhibitors were added to the serosal solution 30 min before histamine or PACAP. The secretion of acid in the isolated stomach was increased by histamine or PACAP, and these responses were totally inhibited by famotidine. IBMX alone increased basal acid secretion and significantly enhanced the acid responses to histamine and PACAP. Among the PDE inhibitors tested, only rolipram (PDE4 inhibitor) significantly increased basal acid secretion and potentiated the acid responses to histamine and PACAP. The latter peptide increased histamine release into the medium, and this response was also enhanced by rolipram. Furthermore, rolipram significantly increased cAMP production induced in the isolated stomach by histamine and PACAP. These results suggest that PDE4 is involved in the local regulation of gastric acid secretion via the degradation of cAMP and that the PDE4 inhibitor rolipram increases the secretion of acid by potentiating acid production in parietal cells and enhancing histamine release from enterochromaffin-like cells.

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  • Role of endothelial nitric oxide synthase in aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats Reviewed

    Shinichi Kato, F. Ohkawa, Y. Ito, K. Amagase, K. Takeuchi

    Journal of Physiology and Pharmacology   60 ( 4 )   147 - 155   2009.12

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    The role of nitric oxide synthase (NOS) isozymes in the aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats was investigated. Two weeks after injection of Freund's complete adjuvant, the animals were given indomethacin, and the stomach was examined for damage 4 h later. Indomethacin caused hemorrhagic lesions in the normal rat stomach, and these lesions were markedly aggravated in arthritic rats. Pretreatment with L-NAME (a nonselective inhibitor of NOS) and aminoguanidine (a relative selective inhibitor of iNOS) did not affect the ulcerogenic response in normal rats but dose-dependently prevented the aggravation of lesions in arthritic rats, but the effect of aminoguanidine was apparently less than that of L-NAME. The increased ulcerogenic response in arthritic rats was significantly suppressed by 1400 W (a selective inhibitor of iNOS) and L-NIO (a selective inhibitor of eNOS) but not by L-NPA (a selective inhibitor of nNOS). The concurrent administration of 1400 W and L-NIO almost totally abolished the aggravation of damage in arthritic rats. The expressions of eNOS and iNOS but not nNOS in the gastric mucosa were clearly enhanced in arthritic rats. Mucosal levels of non-protein sulfhydryls were significantly lower in arthritic rats than those in normal rats. The aggravation of damage in arthritic rats was significantly prevented by glutathione. These results suggest that the increased ulcerogenic response to indomethacin in arthritic rat stomachs is mediated by NO derived from eNOS in addition to iNOS. It is assumed that eNOS/NO may act harmfully on the gastric mucosa of arthritic rats with mucosal SH deficiency.

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  • Dual role of nitric oxide in gastric hypersecretion in the distended stomach: Inhibition of acid secretion and stimulation of pepsinongen secretion Reviewed

    Yasuyuki Ito, Sayaka Okuda, Fumikazu Ohkawa, Shinichi Kato, Shoji Mitsufuji, Toshikazu Yoshikawa, Koji Takeuchi

    LIFE SCIENCES   83 ( 25-26 )   886 - 892   2008.12

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    Aims: We investigate the role of nitric oxide (NO) in the hypersecretion of acid and pepsinogen induced by stomach distension.
    Main method: The rat stomach was distended by instillation of saline through an acute fistula under urethane anesthesia.
    Key findings: Both secretions of acid and pepsinogen were increased by the distension depending on the volume of saline introduced, and responses were attenuated by bilateral cervical vagotomy or prior administration of atropine. N(G)-nitro-L-arginine methyl ester (L-NAME) had a dual effect on these responses, causing an increase in the acid response and a decrease in the pepsin response, both in an L-arginine-sensitive manner. Distension of the stomach increased the luminal NO release; this response was suppressed by vagotomy and L-NAME. Intragastric application of FK409, a NO donor, dose-dependently increased pepsinogen secretion while decreasing acid secretion in the stomach without distension. However, serosal application of both FK409 and 8-bromo-guanosine cyclic 3', 5'-monophosphate (8-Br-cGMP) stimulated the secretion of pepsinogen in isolated mouse stomachs in vitro. The stimulatory effect of FK409 on pepsinogen secretion was totally abolished by LY83583, a guanylate cyclase inhibitor.
    Significance: Distension of the stomach increases both acid and pepsinogen secretion through a vagalcholinergic pathway in addition to the luminal release of NO, and NO affects these responses in opposite ways, suppressing the acid response while enhancing the pepsin response, both mediated by a guanylate cyclase/cGMP pathway. (C) 2008 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.lfs.2008.10.010

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  • Increased susceptibility of small intestine to NSAID-provoked ulceration in rats with adjuvant-induced arthritis: Involvement of enhanced expression of TLR4 Reviewed

    Shinichi Kato, Yasuyuki Ito, Hikaru Nishio, Yoko Aoi, Kikuko Amagase, Koji Takeuchi

    LIFE SCIENCES   81 ( 16 )   1309 - 1316   2007.9

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    NSAIDs damage the small intestine as well as the stomach as adverse effects. We previously reported that the gastric ulcerogenic response to NSAIDs was markedly increased in arthritic rats. The present study was designed to examine the intestinal ulcerogenic property of indomethacin in adjuvant-induced arthritic rats in comparison with normal animals. Arthritis was induced in male Dark Agouti rats by injection of Freund's complete adjuvant into the right hindfoot. Two weeks later, indomethacin was given orally and the intestine was examined for lesions at several time points after indomethacin. Indomethacin produced intestinal lesions in both normal and arthritic rats, but in the latter, the ulcerogenic response occurred much earlier and the severity was markedly enhanced. Amino, guanidine, an inhibitor of iNOS, significantly suppressed the damage, yet the efficacy differed in normal and arthritic rats, depending on the dose schedule; the effect of post-administration (6 h after) was greater than that of pre-administration (0.5 h before) in normal rats, whereas that of post-administration was less than that of pre-administration in arthritic rats. The expression of iNOS and TLR4 in the intestine was enhanced in arthritic rats as compared with normal rats. These results suggest that the intestinal ulcerogenic response to indomethacin is markedly aggravated in arthritic rats. Notably, the onset of the ulceration was much earlier in arthritic rats than normal rats. These phenomena may be accounted for by the upregulation of iNOS/NO through the increased expression of TLR4 in the small intestine of arthritic rats. (c) 2007 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.lfs.2007.08.036

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MISC

  • 定量リン酸化プロテオーム解析が明らかにした末梢神経再生時のGAP-43の新規リン酸化部位

    岡田 正康, 河嵜 麻実, 伊藤 泰行, 吉田 豊, 藤井 幸彦, 五十嵐 道弘

    JSBMS Letters   42 ( Suppl. )   88 - 88   2017.8

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    Language:Japanese   Publisher:(一社)日本医用マススペクトル学会  

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  • Electron Crystallography of Euglenoid Four-Transmembrane Protein Revealed the Linear Polymerization by a Combination of Three-Ways of Intermolecular Interaction

    Hiroshi Suzuki, Yasuyuki Ito, Kazutoshi Tani, Yuji Yamazaki, Masami Uji, Katsuhiko Mineta, Sachiko Tsukita, Yoshinori Fujiyoshi

    BIOPHYSICAL JOURNAL   104 ( 2 )   42A - 42A   2013.1

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  • Pathogenic Importance of Endothelial Isozyme of Nitric Oxide Synthase (eNOS) in Aggravation of Gastric Lesions Induced By Indomethacin and Cold-Restraint Stress in Adjuvant-Induced Arthritic Rats

    Shinichi Kato, Yasuyuki Ito, Fumikazu Ohkawa, Koji Takeuchi

    GASTROENTEROLOGY   136 ( 5 )   A691 - A691   2009.5

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  • Detrimental role of endothelial nitric oxide synthase (eNOS/NNOS3) in aggravation of indomethacin-induced gastric damage in adjuvant arthritis rats

    Shinichi Kato, Yasuyuki Ito, Fumikazu Ohkawa, Kikuko Amagase, Koji Takeuchi

    GASTROENTEROLOGY   134 ( 4 )   A220 - A220   2008.4

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Research Projects

  • 胎生期の神経幹細胞分裂におけるリン酸化タウの役割

    Grant number:23K05975

    2023.4 - 2026.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    伊藤 泰行

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    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

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  • 内因性リン酸化タウを認識する極小分子プローブの開発

    2022.8 - 2023.3

    System name:令和4年度 新潟大学U-go グラント

    伊藤 泰行

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  • 脳発生過程で最も高頻度にチロシンリン酸化されるMAP1Bの機能解明

    2021.9 - 2024.4

    System name:医学系研究奨励

    Awarding organization:武田科学振興財団

    伊藤 泰行

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  • 極長鎖脂肪酸産生による神経軸索成長の制御機構の解明

    Grant number:21K06390

    2021.4 - 2024.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    本多 敦子, 野住 素広, 伊藤 泰行

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    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

    申請者はこれまでに、神経成長円錐の形質膜に脂質マイクロドメイン(脂質ラフト)が多く存在し、そこに集積するシグナル分子の集積・活性化により軸索成長が制御されることを示している。脂質ラフトの形成や機能には極長鎖脂肪酸産生が関与しており、成長円錐には極長鎖脂肪酸産生酵素が多く局在するが、両者の関係性は不明である。そこで申請者は、神経成長円錐での極長鎖脂肪酸産生の、脂質ラフト形成や軸索成長における生理的役割を解明するため、成長円錐に豊富な極長鎖脂肪酸産生酵素 GPSN2に着目し、その欠損マウスを作製・解析を行っている。
    オミクス解析により、GPSN2ノックアウトマウス胎仔脳の成長円錐における脂質(アシル鎖長別)産生・代謝の変化をノンターゲット解析したところ、ノックアウトマウスにおいて極長鎖脂肪酸を含む特定の脂質合成が阻害されていた。
    極長鎖脂肪酸産生阻害による成長円錐の形態・動態変化を解析するため、超解像度顕微鏡および共焦点顕微鏡を用いて、GPSN2ヘテロマウス胎仔脳神経細胞や、脂肪酸伸長酵素shRNAノックダウン神経細胞の成長円錐のイメージング解析を行ったところ、極長鎖脂肪酸産生阻害による成長円錐の形態・動態異常が認められた。同標本における、成長円錐における脂質ラフトの形成や分布の変化を、蛍光標識脂質ラフトマーカーを用いて解析した。
    さらに神経細胞の軸索成長や神経回路形成における変化を細胞、組織レベルで解析するため、成長円錐の形態・動態に変化が見られた細胞における軸索成長の異常をライブイメージングにより解析した。

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  • 神経発生過程で最も高頻度にチロシンリン酸化される微小管結合タンパク質 MAP1B の役割

    2020.7 - 2021.6

    System name:塚田医学奨学会助成金

    Awarding organization:新潟大学塚田医学奨学基金

    伊藤泰行

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  • 高頻度チロシンリン酸化MAP1Bによる神経成長円錐のアクチン骨格制御機構の解明

    Grant number:20K15897

    2020.4 - 2023.3

    System name:科学研究費助成事業 若手研究

    Research category:若手研究

    Awarding organization:日本学術振興会

    伊藤 泰行

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    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

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  • 高頻度チロシンリン酸化MAP1Bが担う神経成長円錐のアクチン骨格制御機構の解明

    2019.11 - 2020.11

    System name:基礎科学研究助成

    Awarding organization:住友財団

    伊藤 泰行

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    Authorship:Principal investigator  Grant type:Competitive

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  • 脳発生過程におけるMAP1Bの高頻度チロシンリン酸化部位の機能解析

    2019.4 - 2021.9

    System name:藤井節郎記念大阪基礎医学研究奨励会助成金

    Awarding organization:藤井節郎記念 大阪基礎医学研究奨励会

    伊藤 泰行

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    Authorship:Principal investigator  Grant type:Competitive

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  • 高頻度チロシンリン酸化MAP1Bが担う神経成長円錐のアクチン骨格制御機構の解明(生体内機能解析)

    2019.4 - 2020.3

    System name:日本人若手研究者研究助成金

    Awarding organization:中島記念国際交流財団

    伊藤 泰行

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    Authorship:Principal investigator  Grant type:Competitive

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  • Roles of the signal transduction via lipid rafts in axon formation and regeneration

    Grant number:18K06480

    2018.4 - 2021.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    HONDA ATSUKO

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    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

    To clarify regulatory mechanisms of the signals for axon formation, we examined the activation system of the signal transduction through the lipid rafts by a membrane protein, M6a in the neuronal growth cones (GC). We analyzed the molecules interacting with M6a on plasma membrane, or the proteins localized in GC lipid rafts via M6a, using proteomic analysis. Our proteomic data showed that M6a interacts with adhesion molecules, e.g. Integrin, the receptors and endoplasmic reticulum on plasma membrane, and recruits some determinants of the neuronal polarity, some kinases, G-proteins and some lipid synthases to lipid rafts. These data indicated that the extra-intra cellular signal transductions and the lipid synthesis in the lipid rafts were intensified by M6a in the GC.

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  • Actin-dependent endocytosis at the leading edge of the growth cone

    Grant number:18K06459

    2018.4 - 2021.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Nozumi Motohiro

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    Grant amount:\4420000 ( Direct Cost: \3400000 、 Indirect Cost:\1020000 )

    Growth cones are essential for proper neural circuit formation and axon regeneration. At the leading edge of the growth cone, the plasma membrane is pushed by the elongation of the actin cytoskeleton, which generates the driving force for axon outgrowth. In this study, we found non-adhesive filopodia extending vertically from the surface of the growth cones by three-dimensional observations using super-resolution microscopy, 3D-SIM. The filopodia showed lipid raft-dependent accumulation of neuropilin-1, an axon guidance receptor, and repeated elongation and retraction within a minute. The growth cone could actively recruit receptors toward the extracellular space through the filopodia elongation, suggesting that they efficiently capture soluble ligands.

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  • 高頻度チロシンリン酸化MAP1B の神経発生における役割

    2018.1 - 2019.4

    System name:研究奨励金

    Awarding organization:上原記念生命科学財団

    伊藤 泰行

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    Authorship:Principal investigator  Grant type:Competitive

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  • 脳発生過程に関与するチロシンリン酸化修飾の網羅的解析と意義解明

    2016.9 - 2019.5

    System name:医学系研究奨励

    Awarding organization:武田科学振興財団

    伊藤 泰行

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    Authorship:Principal investigator  Grant type:Competitive

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  • Claudin類似4回膜貫通タンパク質Euglena-IP39の構造および機能解析

    2011.4 - 2013.3

    System name:特別研究員奨励費

    Awarding organization:日本学術振興会

    伊藤 泰行

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    Authorship:Principal investigator  Grant type:Competitive

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